The Experimental Research Of Communicating Hydrocephalus

Objective To investigate the nosogeny of communicating hydrocephalus with the kaolin-induced hydrocephalus rats using the technique of morphology, immunohistochemistry and imaging. And investigate the correlation about communicating hydrocephalus with the expression of transforming growth factorβ1 (TGF-β1) in the kaolin-induced hydrocephalus rats.Methods To observe the occurrence of subarachnoid fibrosis and the expression of transforming growth factorβ1 in cerebrospinal fluid (CSF) and tissue sections by using the kaolin-induced communicating hydrocephalus rats, and to measure the lateral ventricle volume by CT or MRI imaging. 40 Wistar male rats were randomly divided into two groups, K group were 25 rats (2% kaolin injection group): were injected into the cisterna magna with kaolin 0.1ml under microscope, they were killed after 28 days, collecting cerebrospinal fluid before dead. S group were 15 rats (saline injected group): were injected into the cisterna magna with normal saline group, approach with K group, only the injection of normal saline 0.1ml, were killed after 28 days, collecting cerebrospinal fluid before dead. All brain specimens by immunohistochemical staining in each group and observe the expression of transforming growth factorβ1. To observe and measure the occurrence of subarachnoid fibrosis. To measure the level of transforming growth factorβ1 in cerebrospinal fluid. And measure the lateral ventricle volume by CT or MRI imaging.Results (1) The K group rats were injected into the cisterna magna with 2% kaolin, analysis of ventricle volume'results showed that a total of 22 rats were successfully induced the hydrocephalus, and whose ventricular system expanded as time goes on, the cerebral ventricles were less expanded. The ventricular volume of saline group was similar to that of normal rats, no expansion. (2) The expression of transforming growth factorβ1 in the cerebrospinal fluid was more in group K than in group S. There was significant difference between the two groups. (3) HE staining and Masson staining showed that K group rats cistern magna inflammatory fibrosis occur more extensively than the S group. (4) Masson staining showed that K group rats'abnormal area contains a lot of collagen fibers, the S group didn't like this way. (5) Transforming growth factorβ1 immunohistochemistry staining showed that K group rats'abnormal area expression of transforming growth factorβ1 was stronger than S group.Conclusion (1) The nosogeny of communicating hydrocephalus with the kaolin- induced hydrocephalus rats: When the kaolin injected into the cisterna magna, due to the organism's biological defense system and the mechanism of chronic inflammation, a large number of phagocytic cells into the cerebrospinal fluid to swallow kaolin as foreign bodies. The large number of potential cerebrospinal fluid transforming growth factorβ1 was rapidly activated and microglia also release transforming growth factorβ1 into the cerebrospinal fluid. transforming growth factorβ1 is an inflammatory chemokine, it is caused phagocytic cells aggregate to the kaolin-induced aseptic inflammation area. It is also to stimulate collagen and fibronectin gene expression, so that the collagen fibers proliferate, a vicious cycle formed. Finally the cisterna magna extensive fibrosis and occlusion of subarachnoid adhesions occur, and then leading the cerebrospinal fluid circulation and dynamics disorder caused the communicating hydrocephalus. Therefore, the kaolin-induced hydrocephalus rats model is applicable to study communicating hydrocephalus caused by subarachnoid hemorrhage (SAH) , meningitis. (2)The results of our experimental showed: transforming growth factorβ1 have many function, but there are two role to be sure about kaolin-induced communicating hydrocephalus rat model, one is transforming growth factorβ1 as an inflammatory chemokine, it is caused phagocytic cells aggregate to the kaolin-induced aseptic inflammation area. Another is that transforming growth factorβ1 also stimulate collagen and fibronectin gene expression, so that the collagen fibers proliferate. Therefore, transforming growth factorβ1 intervent could be the a breakthrough of drug therapy on communicating hydrocephalus after subarachnoid hemorrhage.